epimedin-c has been researched along with Osteoporosis* in 2 studies
2 other study(ies) available for epimedin-c and Osteoporosis
Article | Year |
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Epimedin C protects dexamethasone-induced osteoblasts through NRF1/RhoA pathway.
Osteoporosis (OP) is a metabolic bone disease that leads to decrease of bone strength and increase bone brittle and fracture. Dexamethasone (DXMS) usage is a common risk factor of OP. In present study, we found that the Epimedin C protect the DXMS-induced OP, Ras Homolog Family Member A transforming protein (RhoA) was increased in osteoblasts (OBs) and OP models. We further revealed that Nrf1 is a transcription factor that responds to Epimedin C and DXMS in modulating RhoA promoter. The results collectively demonstrate that Epimedin C functions as a positive modifier of RhoA via alteration of Nrf1 transcriptional activity on RhoA promoter, thereby, protecting OBs against OP. Our work is the first study identifying the Epimedin C function in balancing the OBs in OP model via Nrf1-RhoA. Topics: Dexamethasone; Humans; Nuclear Respiratory Factor 1; Osteoblasts; Osteoporosis; rhoA GTP-Binding Protein | 2023 |
[Activity Study of Icarlin and Epimedin C Monomer under the Same Molarity in Osteoporosis Ze- brafish Model].
Objective To evaluate anti-osteoporotic activity of icariin and Epimedin C monomer under the same molarity in predinsolone-induced osteoporosis zebrafish. Methods Zebrafish larvae after 4-day fertilization were divided into group S [0. 5% dimethyl sulfoxide (DMSO) , A (25 μmol/L prednisolone, 0. 5% DMSO), B (2 IU/L salmon calcitonin, 25 μmol/L prednisolone,0. 5% DMSO), C (1. 5 1,mol/L icariin, 25 μmol/L prednisolone, 0. 5% DMSO) , D (15 μLmol/L icariin,25 μmol/L prednisolone, 0. 5% DM- SO), E (150 μmol/L icariin, 25 μmol/L prednisolone, 0. 5% DMSO), F (1. 5 μmol/L Epimediri C, 25 μmol/L prednisolone, 0. 5% DMSO) , G (15 μmol/L Epimedin C, 25 μmol/L prednisolone, 0.5% DM- SO) , H (150 μmol/L Epimedin C, 25 μmol/L prednisolone, 0. 5% DMSO). All culture solution contained 0. 5% DMSO. All the young fishes were grown in a 24-well plate. The culture medium was changed every day. They were cultured in a incubator box at 28. 5 °C and killed at day 9. Zebrafish skeleton was stained with alizarin red. The stained Zebrafish ventral skull was observed using microscope, and mineralized area was quantitatively analyzed. Results Compared with group S, accumulative integrated optical densi- ty(IOD)of the mineralized area significantly decreased in group A (P <0. 01) ; accumulative IOD of the mineralized area significantly increased in group B (P <0. 01). The accumulative IOD of the mineralized area showed weakly increasing tendency in group C, D, and E along with increased concentration (P < 0. 05). Compared with group A, accumulative IOD obviously increased in group B with statistical difference (P <0. 01) , but with no statistical difference as compared with group C or group D (P >0. 05). Statistical difference existed in accumulative IOD between group A and group E (P <0. 05). The mineralized area showed increasing tendency in group F and group G along with increased concentration (P <0. 05), and accumulative IOD obviously increased as well (P <0. 05). No Zebrafish embryo survived in group H. There was no statistical difference in Zebrafish embryo survival among group E, F, or G (P >0. 05). The staining of Zebrafish skull was clearly seen in group S, with vertebrae and bilateral branchial skeleton clearly seen. The intensity of staining in the same area was obviously attenuated in group A. The osteo- genesis was speeded up under the same condition in group B, with obviously enlarged mineralized area and more darkly stained bone tissue. The mineralization of skull was Topics: Animals; Disease Models, Animal; Flavonoids; Glucosides; Osteoporosis; Zebrafish | 2016 |